Cardiac stimulating devices such as pacemakers and cardioverter-defibrillators are well known. A variety of devices are presently available that apply electrical pulses to a patient's heart in order to maintain a healthy heart rhythm. The simplest cardiac stimulating devices apply pacing pulses to the patient's heart at regular predetermined intervals. More sophisticated devices monitor the various heartbeat signals within a patient's heart so that the strength and timing of the electrical pulses applied to the heart can be specifically tailored to the patient's varying needs.
Cardiac stimulating devices contain detection circuitry to sense the patient's internal heartbeat signals via leads connected to the heart. For example, a bipolar lead connected to the patient's ventricle can be used to sense the patient's ventricular heart rate. By analyzing the rate and the stability of the ventricular heartbeat signal, some conventional cardiac stimulating devices are capable of determining whether the patient is suffering from an arrhythmia such as ventricular tachycardia (a condition in which the heart beats too quickly) or fibrillation (a condition in which the heart quivers chaotically).
Cardiac stimulating devices typically differ in the type of stimulation therapy that may be delivered to the patient's heart in response to a detected arrhythmia.
Antitachycardia pacemakers, for example, attempt to terminate detected ventricular tachycardia episodes by applying one or more bursts of fairly weak antitachycardia stimulation pulses to the patient's heart. More sophisticated devices contain cardioversion circuitry, which allows synchronous, higher energy cardioversion stimulation pulses (e.g., 0.5-5 J) to be used to terminate the arrhythmias. Cardiac stimulating devices with defibrillation capabilities can apply higher energy electrical stimulation pulses (e.g., 20-40 J). The various antitachycardia, cardioversion, and defibrillation stimulation pulses that are applied to the heart are all known as "cardiac stimulation therapies."
Typically, the various cardiac therapies are applied to the heart in a tiered fashion. Initial attempts to terminate an arrhythmia use the least aggressive methods such as applying bursts of antitachycardia pulses to the heart. If this fails to terminate the arrhythmia or if the arrhythmia accelerates in rate, a cardioversion shock, or ultimately a defibrillation shock may be applied.
In order to determine whether a patient is suffering from an episode of tachycardia that should be terminated by the application of a suitable therapy, cardiac stimulating devices typically measure the rate of a patient's ventricular heartbeat and monitor its stability. The stability (or regularity of the timing) of a patient's heartbeat from beat to beat is indicative of the patient's cardiac condition, because, as is well known, a normal human heartbeat is somewhat unstable, whereas cardiac arrhythmias--such as tachycardia episodes--are often stable. One of the reasons that many ventricular tachycardia episodes are stable is that they are sometimes caused by electrical heartbeat signals that have recirculated within the heart by a feedback pathway. A tachycardia episode that is caused by the feedback of heartbeat signals tends to be stable. Various algorithms have been developed for determining whether a patient's heartbeat should be classified as "stable". For example, the period of the most recently measured ventricular beat can be compared to the immediately preceding beat, or can be compared to a running average of recent heart beat periods.
If the ventricular heart rate exceeds a predetermined ventricular tachycardia threshold rate (e.g., 150 beats per minute "bpm"), and if the beats are determined to be stable, then appropriate ventricular therapy can be applied to the patient's heart. Although this technique is generally successful for terminating many potentially life-threatening tachycardias, there are some circumstances in which a more sophisticated approach would be preferred.
For example, occasionally a patient's ventricular heartbeat may exceed a predetermined ventricular tachycardia threshold and be relatively stable--normally an indication that ventricular therapy should be applied. It may be, however, that the elevated ventricular heart rate is due to an atrial arrhythmia that has produced electrical signals that have propagated to the ventricle. Atrial arrhythmias are undesirable, but are typically not life-threatening because the ventricles of the heart can continue to effectively pump blood even if the atrial heart chambers beat arrhythmically.
If a patient suffers from an atrial arrhythmia that causes a corresponding ventricular arrhythmia, applying ventricular electrical pulses to the patient's heart will usually be ineffective at terminating the arrhythmia episode. Applying ventricular therapy to the patient's heart in these circumstances may actually be harmful, because the ventricular electrical pulses may initiate a ventricular tachycardia episode or induce fibrillation.
Further, using conventional criteria for detecting ventricular antiarrhythmias, therapies are typically only applied if the ventricular heartbeat is found to be relatively stable using a stability analysis algorithm.
However, occasionally a ventricular arrhythmia may occur that is not sufficiently stable to be confirmed as a ventricular episode using conventional stability algorithms. Some arrhythmia episodes in which ventricular therapy would be appropriate are therefore not treated. These episodes could, however, be detected if atrial and ventricular heartbeat signals were analyzed properly.
What is needed, therefore, is a cardiac stimulating device that does not apply ventricular therapy to a patient's heart if the ventricular heart arrhythmia is due to an atrial arrhythmia condition, but which applies ventricular therapy when an analysis of the patient's ventricular and atrial heart rates indicates that it is proper to do so. If desired, the cardiac stimulating device could also apply atrial therapies to the patient's heart.